Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Export
Filter
  • PROGRESSION  (14)
Collection
Keywords
  • 1
    Keywords: APOPTOSIS ; CANCER ; CELLS ; EXPRESSION ; tumor ; CELL ; human ; MODEL ; DISEASE ; SITES ; GENE ; GENES ; transcription ; MICE ; NF-KAPPA-B ; COMPLEX ; COMPLEXES ; DNA ; MECHANISM ; murine ; TRANSCRIPTION FACTOR ; IMPACT ; animals ; mechanisms ; BINDING ; SEQUENCE ; SEQUENCES ; TARGET ; MOUSE ; STAGE ; TRANSCRIPTION FACTORS ; PROGRESSION ; MALIGNANCIES ; PATTERNS ; PROMOTER ; AGE ; transgenic ; leukemia ; DNA methylation ; TUMOR-SUPPRESSOR GENE ; REGION ; B-CELLS ; RECRUITMENT ; STRATEGIES ; MOUSE MODEL ; TARGETS ; REPRESSION ; METHYLATION ; TRANSCRIPTIONAL REPRESSION ; REGULATOR ; MALIGNANCY ; PROGRAM ; TUMOR-SUPPRESSOR ; CLL ; MURINE MODEL ; development ; BINDING-SITE ; USA ; EPIGENETICS ; ONSET ; CPG-ISLAND METHYLATION ; BINDING-SITES ; OCCURS ; tumor suppressor ; epigenetic ; STATE ; BINDING SITE ; histone modifications ; ABERRANT METHYLATION ; 3 ; therapeutic ; THERAPEUTIC TARGET ; WELL ; STRATEGY ; INVESTIGATE ; RATIONALE ; TRANSCRIPTION-FACTOR ; FOXD3
    Abstract: Epigenetic alterations, including gain or loss of DNA methylation, are a hallmark of nearly every malignancy. Changes in DNA methylation can impact expression of cancer-related genes including apoptosis regulators and tumor suppressors. Because such epigenetic changes are reversible, they are being aggressively investigated as potential therapeutic targets. Here we use the E mu-TCL1 transgenic mouse model of chronic lymphocytic leukemia (CLL) to determine the timing and patterns of aberrant DNA methylation, and to investigate the mechanisms that lead to aberrant DNA methylation. We show that CLL cells from E mu-TCL1 mice at various stages recapitulate epigenetic alterations seen in human CLL. Aberrant methylation of promoter sequences is observed as early as 3 months of age in these animals, well before disease onset. Abnormally methylated promoter regions include binding sites for the transcription factor FOXD3. We show that loss of Foxd3 expression due to an NF-kappa B p50/p50:HDAC1 repressor complex occurs in TCL1-positive B cells before methylation. Therefore, specific transcriptional repression is an early event leading to epigenetic silencing of target genes in murine and human CLL. These results provide strong rationale for the development of strategies to target NF-kappa B components in CLL and potentially other B-cell malignancies
    Type of Publication: Journal article published
    PubMed ID: 19666576
    Signatur Availability
    BibTip Others were also interested in ...
  • 2
    Keywords: CANCER ; CELLS ; EXPRESSION ; IN-VITRO ; INHIBITOR ; tumor ; TUMOR-CELLS ; carcinoma ; CELL ; COMBINATION ; MODEL ; VITRO ; SITE ; SITES ; GENE ; GENE-EXPRESSION ; GENES ; PROTEIN ; TISSUE ; LINES ; DNA ; CARCINOGENESIS ; BREAST ; breast cancer ; BREAST-CANCER ; PROGRESSION ; genetics ; DNA methylation ; inactivation ; PCR ; REGION ; TRANSFORMATION ; EPITHELIAL-CELLS ; CARCINOMAS ; NETHERLANDS ; histone deacetylase inhibitor ; METHYLATION ; HYPERMETHYLATION ; ESTRADIOL ; PATTERN ; SCIENCE ; CPG ISLANDS ; ESTROGEN ; 17-BETA-ESTRADIOL ; EPIGENETIC CHANGES ; MESENCHYMAL TRANSITION ; Genetic ; heregulin ; Cell transformation ; ERBB RECEPTOR FAMILY ; HISTONE-DEACETYLASE INHIBITORS ; Neuregulin
    Abstract: Epigenetic inactivation of genes by DNA hypermethylation plays an important role in carcinogenesis An in vitro model of human breast epithelial cell transformation was used to study epigenetic changes induced by estradiol during the neoplastic process Different stages of tumor initiation and progression are represented in this model being MCF-10F the normal stage; trMCF cells, the transformed stage, bsMCF cells, the invasive stage and, caMCF cells, the tumor stage Global methylation studies by restriction landmark genomic scanning (RLGS) showed an increased DNA methylation during the in the invasive and tumor stages Expression studies showed that NRG1 (neuregulin 1), CSS3 (chondroitin sulfate synthase 3) and SNIP (SNAP-25-interacting protein) were downregulated in the invasive and tumor cells. The transformed cells showed low expression of STXBP6(amysin)compared to the parental cells MCF-10F The treatment of these cells with the demethylating agent 5-aza-dC alone or in combination with the histone deacetylase inhibitor trichostatin increased the expression of NRG1, STXBP6, CSS3 and SNIP confirming that DNA methylation plays an Important role in the regulation of the expression of these genes The NRG1 exon 1 has a region located between -136 and +79 (considering +1, the translational initiation site) rich in CpG sites that was analyzed by methylation specific PCR (MSP) NRG1 exon 1 showed progressive changes in the methylation pattern associated with the progression of the neoplastic process in this model; NRG1 exon 1 was unmethylated in MCF-10F and trMCF cells, becoming hypermethylated in the invasive (bsMCF) and tumor (caMCF) stages Studies of human breast tissue samples showed that NRG1 exon 1 was partially methylated in 14 out of 17 (82.4%) invasive carcinomas although it was unmethylated in normal tissues (8 out of 10 normal breast tissue samples) Furthermore, NRG1 exon 1 was partially methylated in 9 out of 14(64.3%) morphologically normal tissue samples adjacent to invasive carcinomas. (C) 2010 Elsevier B V. All rights reserved
    Type of Publication: Journal article published
    PubMed ID: 20193695
    Signatur Availability
    BibTip Others were also interested in ...
  • 3
    Keywords: CANCER ; PATHWAY ; GENE-EXPRESSION ; TRANSCRIPTION FACTOR ; PROGRESSION ; chemotherapy ; EMBRYONIC STEM-CELLS ; PROMOTER HYPERMETHYLATION ; AML ; TUMOR-NECROSIS
    Abstract: BACKGROUND: Aberrant DNA methylation is frequently found in human malignancies including acute myeloid leukemia (AML). While most studies focus on later disease stages, the onset of aberrant DNA methylation events and their dynamics during leukemic progression are largely unknown. METHODS: We screened genome-wide for aberrant CpG island methylation in three disease stages of a murine AML model that is driven by hypomorphic expression of the hematopoietic transcription factor PU.1. DNA methylation levels of selected genes were correlated with methylation levels of CD34+ cells and lineage negative, CD127-, c-Kit+, Sca-1+ cells; common myeloid progenitors; granulocyte-macrophage progenitors; and megakaryocyte-erythroid progenitors. RESULTS: We identified 1,184 hypermethylated array probes covering 762 associated genes in the preleukemic stage. During disease progression, the number of hypermethylated genes increased to 5,465 in the late leukemic disease stage. Using publicly available data, we found a significant enrichment of PU.1 binding sites in the preleukemic hypermethylated genes, suggesting that shortage of PU.1 makes PU.1 binding sites in the DNA accessible for aberrant methylation. Many known AML associated genes such as RUNX1 and HIC1 were found among the preleukemic hypermethylated genes. Nine novel hypermethylated genes, FZD5, FZD8, PRDM16, ROBO3, CXCL14, BCOR, ITPKA, HES6 and TAL1, the latter four being potential PU.1 targets, were confirmed to be hypermethylated in human normal karyotype AML patients, underscoring the relevance of the mouse model for human AML. CONCLUSIONS: Our study identified early aberrantly methylated genes as potential contributors to onset and progression of AML.
    Type of Publication: Journal article published
    PubMed ID: 24944583
    Signatur Availability
    BibTip Others were also interested in ...
  • 4
    facet.materialart.
    Unknown
    HNO 56 (6), 594-602 
    Keywords: CANCER ; EXPRESSION ; SURVIVAL ; tumor ; carcinoma ; CELL ; Germany ; THERAPY ; DISEASE ; NEW-YORK ; SITES ; GENE ; GENES ; DNA ; BIOMARKERS ; SEQUENCE ; SEQUENCES ; ALPHA ; prevention ; PROGRESSION ; ASSAY ; DNA methylation ; inactivation ; TUMOR-SUPPRESSOR GENE ; REGION ; REGIONS ; PHENOTYPE ; SQUAMOUS-CELL CARCINOMA ; HEAD ; CARCINOMAS ; STRATEGIES ; squamous cell carcinoma ; OUTCOMES ; HYPERMETHYLATION ; C/EBP-ALPHA ; molecular ; CELL CARCINOMA ; TUMOR-SUPPRESSOR ; THERAPIES ; CANDIDATE GENES ; HNSCC ; CPG ISLANDS ; biomarker ; SUPPRESSOR ; PROMOTER HYPERMETHYLATION ; USA ; LOSSES ; EPIGENETICS ; CANDIDATE ; CANCERS ; REDUCED EXPRESSION ; DNA-METHYLATION ; modification ; tumor suppressor ; epigenetic ; DNA METHYLATION PATTERNS
    Abstract: For years, head and neck squamous cell carcinomas (HNSCC) have been among the leading cancers worldwide. Despite considerable efforts, the 5-year survival rate for HNSCC has not changed significantly. To improve this situation, it is necessary to understand the fundamental biological processes leading to the disease and its progression. In addition to known genetic changes in HNSCC, molecular cytogenetic investigations have identified chromosomal regions of gains and losses, but many of the responsible candidate genes have yet to be identified. Furthermore, recent results indicate the importance of epigenetic modifications in HNSCC, such as DNA methylation. Several genes, including the tumor suppressor CDKN2A and other candidates such as DAPK1, MGMT, TIMP3, TCF21, and C/EBP alpha, have been found to harbor hypermethylated regulatory sequences that lead to reduced expression or gene silencing. Hypermethylation in such genes could be used not only as biomarkers for the early detection of HNSCC but also to improve prevention strategies and therapy outcomes
    Type of Publication: Journal article published
    PubMed ID: 18483718
    Signatur Availability
    BibTip Others were also interested in ...
  • 5
    Keywords: RECEPTOR ; CANCER ; EXPRESSION ; GROWTH ; GROWTH-FACTOR ; INHIBITOR ; tumor ; CELL ; FACTOR RECEPTOR ; INHIBITION ; KINASE ; COMMON ; GENE ; GENE-EXPRESSION ; GENES ; PROTEIN ; meningioma ; TUMORS ; DNA ; MECHANISM ; mechanisms ; PROTEIN-KINASE ; IDENTIFICATION ; PROGRESSION ; COPY NUMBER ; gene expression ; MUTATION ; CELL-LINE ; DNA methylation ; inactivation ; MUTATIONS ; METHYLATION ; EPIDERMAL-GROWTH-FACTOR ; signaling ; SAN-FRANCISCO ; TUMOR-SUPPRESSOR ; development ; LOCUS ; MENINGIOMAS ; USA ; epidermal growth factor receptor ; GROWTH-FACTOR-RECEPTOR ; LOCI ; ANAPLASTIC MENINGIOMAS ; tumor suppressor ; epigenetic ; ABERRANT METHYLATION ; Genetic ; METHYLATION INHIBITOR ; tumor grade ; EPIDERMAL-GROWTH ; CODING SEQUENCES ; COLONIES ; MENINGIOMA CELL-LINE ; METHYLATION STATUS ; restriction landmark genome scanning ; WNK2
    Abstract: Both genetic and epigenetic mechanisms contribute to meningioma development by altering gene expression and protein function. To determine the relative contribution of each mechanism to meningioma development, we used an integrative approach measuring copy number and DNA methylation changes genomewide. We found that genetic alterations affected 1.9%, 7.4%, and 13.3% of the 691 loci studied, whereas epigenetic mechanisms affected 5.4%, 9.9%, and 10.3% of these loci in grade I, II, and III meningiomas, respectively. Genetic and epigenetic mechanisms rarely involved the same locus in any given tumor. The predilection for epigenetic rather than genetic silencing was exemplified at the 5' CpG island of WNK2, a serine-threonine kinase gene on chromosome 9q22.31. WNK2 is known to negatively regulate epidermal growth factor receptor signaling via inhibition of MEK1 (mitogen-activated protein kinase kinase 1), and point mutations have been reported in WNK1, WNK2, WNK3, and WNK4. In meningiomas, WNK2 was aberrantly methylated in 83% and 71% of grade II and III meningiomas, respectively, but rarely in a total of 209 tumors from 13 other tumor types. Aberrant methylation of the CpG island was associated with decreased expression in primary tumors. WNK2 could be reactivated with a methylation inhibitor in IOMM-Lee, a meningioma cell line with a densely methylated WNK2 CpG island and lack of WNK2 expression. Expression of exogenous WNK2 inhibited colony formation, implicating it as a potential cell growth suppressor. These findings indicate that epigenetic mechanisms are common across meningiomas of all grades and that for specific genes such as WNK2, epigenetic alteration may be the dominant, grade-specific mechanism of gene inactivation. Neuro-Oncology 11, 414-422, 2009 (Posted to Neuro-Oncology [serial online], Doc. D08-00170, November 11, 2008. URL http://neuro-oncology.dukejournals.org; DOI: 10.1215/15228517-2008-096)
    Type of Publication: Journal article published
    PubMed ID: 19001526
    Signatur Availability
    BibTip Others were also interested in ...
  • 6
    Keywords: CELLS ; EXPRESSION ; GROWTH ; DIFFERENTIATION ; PROGRESSION ; REPRESSION ; NASOPHARYNGEAL CARCINOMA ; GROUP PROTEIN EZH2 ; POLYCOMB ; GENE FUSIONS
    Abstract: Prostate cancer is the second most common cancer among men worldwide. Alterations in the DNA methylation pattern can be one of the leading causes for prostate cancer formation. This study is the first high-throughput sequencing study investigating genome-wide DNA methylation patterns in a large cohort of 51 tumor and 53 benign prostate samples using methylated DNA immunoprecipitation sequencing. Comparative analyses identified more than 147,000 cancer-associated epigenetic alterations. In addition, global methylation patterns show significant differences based on the TMPRSS2-ERG rearrangement status. We propose the hypermethylation of miR-26a as an alternative pathway of ERG rearrangement-independent EZH2 activation. The observed increase in differential methylation events in fusion-negative tumors can explain the tumorigenic process in the absence of genomic rearrangements. SIGNIFICANCE: In contrast to TMPRSS2-ERG -rearranged tumors, the pathomechanism for gene fusion-negative tumors is completely unclear. Using a sequencing-based approach, our work uncovers significant global epigenetic alterations in TMPRSS2-ERG gene fusion-negative tumors and provides a mechanistic explanation for the tumor formation process.
    Type of Publication: Journal article published
    PubMed ID: 22930729
    Signatur Availability
    BibTip Others were also interested in ...
  • 7
    Keywords: RECEPTOR ; MECHANISM ; DELETION ; PROGRESSION ; MEN ; MYELOID-LEUKEMIA ; REARRANGEMENTS ; GENE FUSIONS ; SEQUENCING DATA ; PSA RECURRENCE
    Abstract: Early-onset prostate cancer (EO-PCA) represents the earliest clinical manifestation of prostate cancer. To compare the genomic alteration landscapes of EO-PCA with "classical" (elderly-onset) PCA, we performed deep sequencing-based genomics analyses in 11 tumors diagnosed at young age, and pursued comparative assessments with seven elderly-onset PCA genomes. Remarkable age-related differences in structural rearrangement (SR) formation became evident, suggesting distinct disease pathomechanisms. Whereas EO-PCAs harbored a prevalence of balanced SRs, with a specific abundance of androgen-regulated ETS gene fusions including TMPRSS2:ERG, elderly-onset PCAs displayed primarily non-androgen-associated SRs. Data from a validation cohort of 〉 10,000 patients showed age-dependent androgen receptor levels and a prevalence of SRs affecting androgen-regulated genes, further substantiating the activity of a characteristic "androgen-type" pathomechanism in EO-PCA.
    Type of Publication: Journal article published
    PubMed ID: 23410972
    Signatur Availability
    BibTip Others were also interested in ...
  • 8
    Keywords: PATHWAYS ; BREAST-CANCER ; PROGRESSION ; SIGNAL-TRANSDUCTION ; TUMOR-SUPPRESSOR GENE ; PTEN ; MAPK ; TUMORIGENESIS ; BETA-ACTIVATED KINASE-1 ; TAK1
    Abstract: 6q12-22 is the second most commonly deleted genomic region in prostate cancer. Mapping studies have described a minimally deleted area at 6q15, containing MAP3K7/TAK1, which was recently shown to have tumor suppressive properties. To determine prevalence and clinical significance of MAP3K7 alterations in prostate cancer, a tissue microarray containing 4699 prostate cancer samples was analyzed by fluorescence in situ hybridization. Heterozygous MAP3K7 deletions were found in 18.48% of 2289 interpretable prostate cancers. MAP3K7 deletions were significantly associated with advanced tumor stage (P〈0.0001), high Gleason grade (P〈0.0001), lymph node metastasis (P〈0.0108) and early biochemical recurrence (P〈0.0001). MAP3K7 alterations were typically limited to the loss of one allele as homozygous deletions were virtually absent and sequencing analyses revealed no evidence for MAP3K7 mutations in 15 deleted and in 14 non-deleted cancers. There was a striking inverse association of MAP3K7 deletions and TMPRSS2:ERG fusion status with 26.7% 6q deletions in 1125 ERG-negative and 11.1% 6q deletions in 1198 ERG-positive cancers (P〈0.0001). However, the strong prognostic role of 6q deletions was retained in both ERG-positive and ERG-negative cancers (P〈0.0001 each). In summary, our study identifies MAP3K7 deletion as a prominent feature in ERG-negative prostate cancer with strong association to tumor aggressiveness. MAP3K7 alterations are typically limited to one allele of the gene. Together with the demonstrated tumor suppressive function in cell line experiments and lacking evidence for inactivation through hypermethylation, these results indicate MAP3K7 as a gene for which haploinsufficency is substantially tumorigenic.
    Type of Publication: Journal article published
    PubMed ID: 23370768
    Signatur Availability
    BibTip Others were also interested in ...
  • 9
    Keywords: CANCER ; CELLS ; EXPRESSION ; tumor ; TUMOR-CELLS ; CELL ; human ; IN-VIVO ; MODEL ; MODELS ; VIVO ; CLASSIFICATION ; COMMON ; DISEASE ; DISTINCT ; GENE ; SAMPLE ; SAMPLES ; transcription ; TISSUE ; TUMORS ; DNA ; MECHANISM ; mechanisms ; T cell ; T-CELL ; BIOLOGY ; SEQUENCE ; SEQUENCES ; SUSCEPTIBILITY ; BREAST-CANCER ; culture ; MOUSE ; STAGE ; PROGRESSION ; LYMPHOMA ; PATTERNS ; PROMOTER ; TUMOR PROGRESSION ; genetics ; COLORECTAL-CANCER ; DNA methylation ; inactivation ; p53 ; EVOLUTION ; PHENOTYPE ; MOUSE MODEL ; SELECTION ; specificity ; OVEREXPRESSION ; METHYLATION ; TUMOR CELLS ; heredity ; CHRONIC LYMPHOCYTIC-LEUKEMIA ; HYPERMETHYLATION ; HETEROGENEITY ; EPIGENETIC INACTIVATION ; targeting ; PROGRAM ; PATTERN ; TUMOR-SUPPRESSOR ; HUMAN CANCER ; ACUTE MYELOID-LEUKEMIA ; LIBRARIES ; CELL LYMPHOMA ; CPG ISLANDS ; GENE-TRANSCRIPTION ; development ; TUMOR-CELL ; SUPPRESSOR ; PROFILES ; EVENTS ; SIGNATURE ; DISEASE PROGRESSION ; USA ; CPG ISLAND HYPERMETHYLATION ; HUMAN CANCERS ; PROMOTER METHYLATION ; CANCERS ; in vivo ; genomic ; GENETIC ALTERATION ; RARE ; PREDICT ; CpG island ; MYC ; TUMOR-DEVELOPMENT ; DNA-METHYLATION ; scanning ; CELL LYMPHOMAS ; evidence ; TUMOR SUPPRESSORS ; CAUSAL ROLE ; DNA HYPOMETHYLATION
    Abstract: Hypermethylation of CpG islands is a common epigenetic alteration associated with cancer. Global patterns of hypermethylation are tumor-type specific and nonrandom. The biological significance and the underlying mechanisms of tumor-specific aberrant promoter methylation remain unclear, but some evidence suggests that this specificity involves differential sequence susceptibilities, the targeting of DNA methylation activity to specific promoter sequences, or the selection of rare DNA methylation events during disease progression. Using restriction landmark genomic scanning on samples derived from tissue culture and in vivo models of T cell lymphomas, we found that MYC overexpression gave rise to a specific signature of CpG island hypermethylation. This signature reflected gene transcription profiles and was detected only in advanced stages of disease. The further inactivation of the Pten, p53, and E2f2 tumor suppressors in MYC-induced lymphomas resulted in distinct and diagnostic CpG island methylation signatures. Our data suggest that tumor-specific DNA methylation in lymphomas arises as a result of the selection of rare DNA methylation events during the course of tumor development. This selection appears to be driven by the genetic configuration of tumor cells, providing experimental evidence for a causal role of DNA hypermethylation in tumor progression and an explanation for the tremendous epigenetic heterogeneity observed in the evolution of human cancers. The ability to predict genome-wide epigenetic silencing based on relatively few genetic alterations will allow for a more complete classification of tumors and understanding of tumor cell biology
    Type of Publication: Journal article published
    PubMed ID: 17907813
    Signatur Availability
    BibTip Others were also interested in ...
  • 10
    Keywords: RECEPTOR ; EXPRESSION ; tumor ; CELL ; human ; KINASE ; MODEL ; MODELS ; TYROSINE KINASE ; GENE ; GENES ; TUMORS ; MICE ; DNA ; FAMILY ; TISSUES ; BIOLOGY ; MEMBER ; MOLECULAR-BIOLOGY ; FORM ; ISOFORM ; MOUSE ; TRANSGENIC MICE ; PROGRESSION ; LYMPHOMA ; MALIGNANCIES ; MUTATION ; TUMOR PROGRESSION ; METASTASIS ; genetics ; COLORECTAL-CANCER ; DNA methylation ; LYMPHOCYTES ; MUTATIONS ; ADHESION ; B-CELLS ; ONCOGENE ; TRANSFORMATION ; Jun ; TRANSLOCATION ; REVEALS ; RECEPTORS ; METHYLATION ; heredity ; CHRONIC LYMPHOCYTIC-LEUKEMIA ; B-CELL LYMPHOMA ; HYPERMETHYLATION ; molecular biology ; molecular ; ONCOLOGY ; aberrant expression ; FAMILIES ; MALIGNANT PROGRESSION ; TYROSINE KINASES ; non-Hodgkin lymphoma ; SUBTYPES ; USA ; INVASIVENESS ; B-LYMPHOCYTES ; genomic ; B-CELL ; ENGLAND ; SET ; germinal center ; MULTIPLE GENES ; receptor tyrosine kinase ; RECEPTOR TYROSINE KINASES ; NON-HODGKIN-LYMPHOMA ; MYC ; DNA-METHYLATION ; scanning ; B cells ; COMPLEMENT ; ACTIVATING MUTATION ; EPHRINS ; TCL1 ; TCL1 EXPRESSION
    Abstract: Most human lymphomas originate from transformed germinal center (GC) B lymphocytes. While activating mutations and translocations of MYC, BCL2 and BCL6 promote specific GC lymphoma subtypes, other genetic and epigenetic modi. cations that contribute to malignant progression in the GC remain poorly defined. Recently, aberrant expression of the TCL1 proto-oncogene was identified in major GC lymphoma subtypes. TCL1 transgenic mice offer unique models of both aggressive GC and marginal zone B-cell lymphomas, further supporting a role for TCL1 in B-cell transformation. Here, restriction landmark genomic scanning was employed to discover tumor-associated epigenetic alterations in malignant GC and marginal zone B-cells in TCL1 transgenic mice. Multiple genes were identified that underwent DNA hypermethylation and decreased expression in TCL1 transgenic tumors. Further, we identified a secreted isoform of EPHA7, a member of the Eph family of receptor tyrosine kinases that are able to influence tumor invasiveness, metastasis and neovascularization. EPHA7 was hypermethylated and repressed in both mouse and human GC B-cell non-Hodgkin lymphomas, with the potential to influence tumor progression and spread. These data provide the first set of hypermethylated genes with the potential to complement TCL1-mediated GC B-cell transformation and spread
    Type of Publication: Journal article published
    PubMed ID: 17260020
    Signatur Availability
    BibTip Others were also interested in ...
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...